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龙胆苦苷可改善软骨细胞脂多糖诱导的炎症反应和肥大。

Gentiopicroside ameliorates the lipopolysaccharide-induced inflammatory response and hypertrophy in chondrocytes.

机构信息

School of Special Education and Rehabilitation, Binzhou Medical University, Yantai, Shandong, China.

Department of Rehabilitation, Binzhou Medical University Hospital, Binzhou, Shandong, China.

出版信息

J Orthop Surg Res. 2024 Mar 25;19(1):198. doi: 10.1186/s13018-024-04676-1.

Abstract

PURPOSE

This study aimed to evaluate the protective effects of gentiopicroside against lipopolysaccharide-induced chondrocyte inflammation.

METHODS

SW 1353 chondrosarcoma cells were stimulated with LPS (5 μg/ml) for 24 h and treated with different concentrations of gentiopicroside (GPS) for 24 h. The toxic effects of GPS on chondrocytes were determined using a CCK-8 assay and EdU staining. Western blotting, qPCR, and immunofluorescence analysis were used to examine the protective effect of GPS against the inflammatory response in chondrocytes induced by lipopolysaccharide (LPS). One-way ANOVA was used to compare the differences between the groups (significance level of 0.05).

RESULTS

The CCK-8 results showed that 10, 20 and 40 μM GPS had no significant toxic effects on chondrocytes; GPS effectively reduced the production of IL-1β and PGE2, reversed LPS-induced extracellular matrix degradation in cartilage by inhibiting the Stat3/Runx2 signaling pathway, and suppressed the hypertrophic transformation of SW 1353 chondrosarcoma cells.

CONCLUSION

Our study demonstrated that GPS significantly inhibited the LPS-induced inflammatory response and hypertrophic cellular degeneration in SW 1353 chondrosarcoma cells and is a valuable traditional Chinese medicine for the treatment of knee osteoarthritis.

摘要

目的

本研究旨在评估龙胆苦苷对脂多糖诱导的软骨细胞炎症的保护作用。

方法

用 LPS(5μg/ml)刺激 SW 1353 软骨肉瘤细胞 24 h,并用不同浓度的龙胆苦苷(GPS)处理 24 h。CCK-8 检测和 EdU 染色法测定 GPS 对软骨细胞的毒性作用。Western blot、qPCR 和免疫荧光分析用于检测 GPS 对脂多糖(LPS)诱导的软骨细胞炎症反应的保护作用。采用单因素方差分析比较组间差异(显著性水平为 0.05)。

结果

CCK-8 结果表明,10、20 和 40 μM GPS 对软骨细胞无明显毒性作用;GPS 能有效降低 IL-1β 和 PGE2 的产生,通过抑制 Stat3/Runx2 信号通路逆转 LPS 诱导的软骨细胞外基质降解,并抑制 SW 1353 软骨肉瘤细胞的肥大转化。

结论

本研究表明,GPS 能显著抑制 LPS 诱导的 SW 1353 软骨肉瘤细胞炎症反应和肥大性细胞退变,是治疗膝骨关节炎的一种有价值的中药。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d828/10962176/47403c2b0ef4/13018_2024_4676_Fig1_HTML.jpg

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